Special Issue "Toxins and Virulence Factors of Listeria monocytogenes"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Bacterial Toxins".

Deadline for manuscript submissions: 15 February 2020.

Special Issue Editors

Dr. Didier Cabanes
E-Mail Website
Guest Editor
i3S - Instituto de Investigação e Inovação em Saúde, IBMC - Institute for Molecular and Cell Biology, Rua Alfredo Allen, 208, 4200-135 Porto, Portugal
Interests: Host-pathogen interactions; Bacterial virulence factors; bacterial pore forming toxins, Listeria monocytogenes
Dr. Sandra Sousa
E-Mail Website
Guest Editor
i3S – Instituto de Investigação e Inovação em Saúde, IBMC – Institute for Molecular and Cell Biology, Rua Alfredo Allen, 208, 4200-135 Porto, Portugal
Interests: Pore-forming toxins; host cytoskeleton; Listeria monocytogenes; host–pathogen interactions

Special Issue Information

Dear Colleagues,

Listeria monocytogenes is a major intracellular foodborne bacterial pathogen which causes listeriosis, a human systemic infection. Among zoonotic diseases under EU-surveillance, listeriosis is the most severe. L. monocytogenes can grow under temperatures ranging from 0 to 45°C, in acidic medium and at high osmolarity; conditions that it may encounter in nature, in the food chain, as well as during infection. L. monocytogenes has the capacity to colonize various niches, from inert and organic matrixes to the intestinal lumen where it competes with resident microbiota, translocates across the epithelium, multiplies in phagocytic and non-phagocytic cells, and disseminates via the blood. To adapt and resist to this diversity of environments, L. monocytogenes evolved an arsenal of virulence mechanisms spatially and timely regulated.

Toxins are essential determinants of bacterial virulence. The cholesterol-dependent cytotoxin Listeriolysin O (LLO) is a major L. monocytogenes virulence factor that mediates the escape of bacteria from internalization vacuoles, allowing replication in the cytosol. Other L. monocytogenes toxins have been described to date, including phospholipases (PlcA, PlcB) that contribute to the escape from the endocytic and secondary vacuoles, the thiazole/oxazole-modified toxin Listeriolysin S (LLS) that behaves as a bacteriocin favoring intestinal colonization, or the toxin/antitoxin MazEF involved in growth and survival under stress. In addition, several L. monocytogenes secreted or surface-associated proteins play major roles in virulence.

The L. monocytogenes genome encodes a large number of proteins of still unknown functions; some of them are probably undiscovered virulence factors. This Special Issue focuses on the role of known or new L. monocytogenes determinants acting as offensive or defensive factors but providing benefits to bacterial virulence, with a special emphasis on toxins and secreted or surface proteins. Original research manuscripts, methods, opinions, reviews, and mini reviews are welcome.

Dr. Didier Cabanes
Dr. Sandra Sousa
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Listeria monocytogenes
  • Toxins
  • Virulence factors
  • Surface proteins
  • Secreted proteins
  • Host-pathogen interactions

Published Papers (4 papers)

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Research

Open AccessArticle
A Structural Study on the Listeria Monocytogenes Internalin A—Human E-cadherin Interaction: A Molecular Tool to Investigate the Effects of Missense Mutations
Toxins 2020, 12(1), 60; https://doi.org/10.3390/toxins12010060 - 20 Jan 2020
Abstract
Listeria monocytogenes is a widespread foodborne pathogen of high concern and internalin A is an important virulence factor that mediates cell invasion upon the interaction with the host protein E-cadherin. Nonsense mutations of internalin A are known to reduce virulence. Although missense mutations [...] Read more.
Listeria monocytogenes is a widespread foodborne pathogen of high concern and internalin A is an important virulence factor that mediates cell invasion upon the interaction with the host protein E-cadherin. Nonsense mutations of internalin A are known to reduce virulence. Although missense mutations are largely overlooked, they need to be investigated in respect to their effects in cell invasion processes. This work presented a computational workflow to early characterize internalin A missense mutations. The method reliably estimated the effects of a set of engineered missense mutations in terms of their effects on internalin A–E-cadherin interaction. Then, the effects of mutations of an internalin A variant from a L. monocytogenes isolate were calculated. Mutations showed impairing effects on complex stability providing a mechanistic explanation of the low cells invasion capacity previously observed. Overall, our results provided a rational approach to explain the effects of internalin A missense mutations. Moreover, our findings highlighted that the strength of interaction may not directly relate to the cell invasion capacity reflecting the non-exclusive role of internalin A in determining the virulence of L. monocytogenes. The workflow could be extended to other virulence factors providing a promising platform to support a better molecular understanding of L. monocytogenes epidemiology. Full article
(This article belongs to the Special Issue Toxins and Virulence Factors of Listeria monocytogenes)
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Open AccessArticle
An Inducible Cre-lox System to Analyze the Role of LLO in Listeria monocytogenes Pathogenesis
Toxins 2020, 12(1), 38; https://doi.org/10.3390/toxins12010038 (registering DOI) - 07 Jan 2020
Abstract
Listeriolysin O (LLO) is a pore-forming cytolysin that allows Listeria monocytogenes to escape from phagocytic vacuoles and enter the host cell cytosol. LLO is expressed continuously during infection, but it has been a challenge to evaluate the importance of LLO secreted in the [...] Read more.
Listeriolysin O (LLO) is a pore-forming cytolysin that allows Listeria monocytogenes to escape from phagocytic vacuoles and enter the host cell cytosol. LLO is expressed continuously during infection, but it has been a challenge to evaluate the importance of LLO secreted in the host cell cytosol because deletion of the gene encoding LLO (hly) prevents localization of L. monocytogenes to the cytosol. Here, we describe a L. monocytogenes strain (hlyfl) in which hly is flanked by loxP sites and Cre recombinase is under the transcriptional control of the L. monocytogenes actA promoter, which is highly induced in the host cell cytosol. In less than 2 h after infection of bone marrow-derived macrophages (BMMs), bacteria were 100% non-hemolytic. hlyfl grew intracellularly to levels 10-fold greater than wildtype L. monocytogenes and was less cytotoxic. In an intravenous mouse model, 90% of bacteria were non-hemolytic within three hours in the spleen and eight hours in the liver. The loss of LLO led to a 2-log virulence defect in the spleen and a 4-log virulence defect in the liver compared to WT L. monocytogenes. Thus, the production of LLO in the cytosol has significant impact on the pathogenicity of L. monocytogenes. Full article
(This article belongs to the Special Issue Toxins and Virulence Factors of Listeria monocytogenes)
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Open AccessArticle
Large-Scale Comparison of Toxin and Antitoxins in Listeria monocytogenes
Toxins 2020, 12(1), 29; https://doi.org/10.3390/toxins12010029 - 02 Jan 2020
Abstract
Toxin–antitoxin systems (TASs) are widely distributed in prokaryotes and encode pairs of genes involved in many bacterial biological processes and mechanisms, including pathogenesis. The TASs have not been extensively studied in Listeria monocytogenes (Lm), a pathogenic bacterium of the Firmicutes phylum [...] Read more.
Toxin–antitoxin systems (TASs) are widely distributed in prokaryotes and encode pairs of genes involved in many bacterial biological processes and mechanisms, including pathogenesis. The TASs have not been extensively studied in Listeria monocytogenes (Lm), a pathogenic bacterium of the Firmicutes phylum causing infections in animals and humans. Using our recently published TASmania database, we focused on the known and new putative TASs in 352 Listeria monocytogenes genomes and identified the putative core gene TASs (cgTASs) with the Pasteur BIGSdb-Lm database and, by complementarity, the putative accessory gene TAS (acTASs). We combined the cgTASs with those of an additional 227 L. monocytogenes isolates from our previous studies containing metadata information. We discovered that the differences in 14 cgTAS alleles are sufficient to separate the four main lineages of Listeria monocytogenes. Analyzing these differences in more details, we uncovered potentially co-evolving residues in some pairs of proteins in cgTASs, probably essential for protein–protein interactions within the TAS complex. Full article
(This article belongs to the Special Issue Toxins and Virulence Factors of Listeria monocytogenes)
Open AccessArticle
Validation of Predicted Virulence Factors in Listeria monocytogenes Identified Using Comparative Genomics
Toxins 2019, 11(9), 508; https://doi.org/10.3390/toxins11090508 - 30 Aug 2019
Abstract
Listeria monocytogenes is an intracellular facultative pathogen that causes listeriosis, a foodborne zoonotic infection. There are differences in the pathogenic potential of L. monocytogenes subtypes and strains. Comparison of the genome sequences among L. monocytogenes pathogenic strains EGD-e and F2365 with nonpathogenic L. [...] Read more.
Listeria monocytogenes is an intracellular facultative pathogen that causes listeriosis, a foodborne zoonotic infection. There are differences in the pathogenic potential of L. monocytogenes subtypes and strains. Comparison of the genome sequences among L. monocytogenes pathogenic strains EGD-e and F2365 with nonpathogenic L. innocua CLIP1182 and L. monocytogenes strain HCC23 revealed a set of proteins that were present in pathogenic strains and had no orthologs among the nonpathogenic strains. Among the candidate virulence factors are five proteins: putrescine carbamoyltransferase; InlH/InlC2 family class 1 internalin; phosphotransferase system (PTS) fructose transporter subunit EIIC; putative transketolase; and transcription antiterminator BglG family. To determine if these proteins have a role in adherence and invasion of intestinal epithelial Caco-2 cells and/or contribute to virulence, five mutant strains were constructed. F2365ΔinlC2, F2365Δeiic, and F2365Δtkt exhibited a significant (p < 0.05) reduction in adhesion to Caco-2 cells compared to parent F2365 strain. The invasion of F2365ΔaguB, F2365ΔinlC2, and F2365ΔbglG decreased significantly (p < 0.05) compared with the parent strain. Bacterial loads in mouse liver and spleen infected by F2365 was significantly (p < 0.05) higher than it was for F2365ΔaguB, F2365ΔinlC2, F2365Δeiic, F2365Δtkt, and F2365ΔbglG strains. This study demonstrates that aguB, inlC2, eiic, tkt, and bglG play a role in L. monocytogenes pathogenicity. Full article
(This article belongs to the Special Issue Toxins and Virulence Factors of Listeria monocytogenes)
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